Abstract
Previous models of saccades use circuits with simple elements. Medium-lead burst neurons (MLBNs) fire only during saccades, and generate the eye velocity command. Omnipause neurons (OPNs) fire during fixation and pause during saccades in all directions. OPNs are assumed to inhibit MLBNs. MLBNs have been modeled with a single membrane time constant and a firing rate saturation. Therefore, circuit properties, and not properties of the neurons themselves, determine the dynamical properties of saccades. However, a recent study suggests that MLBNs may have another membrane property, post-inhibitory rebound depolarization, which plays a critical role in the generation of oscillations. This finding raises the question of the effect of OPN offset and rebound depolarization of MLBNs on saccades, because chemical lesions of the OPN region alter the dynamics of saccades. A new model with MLBNs that have two biophysical properties, post-inhibitory rebound depolarization and a threshold, produces behavioral changes in saccades after simulated OPN lesion that are consistent with experiment. We suggest that biophysical properties of MLBNs may contribute to dynamical properties of saccades, such as speed and latency.
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